ArticleCell death and differentiation2017
Inhibition of Twist1-mediated invasion by Chk2 promotes premature senescence in p53-defective cancer cells.
Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- Impact of the ATM/Chk2 pathway and cell cycle phase on radiation-induced senescence in A549 human lung cancer cells.Biomedical reports · 2025Article
- Comprehensive assessment of cellular senescence in intestinal immunity and biologic therapy response in ulcerative colitis.Scientific reports · 2024Article
- MiR-34b promotes oxidative stress and induces cellular senescence through TWIST1 in human cervical cancer.Translational oncology · 2024Article
- Cellular senescence: Neither irreversible nor reversible.The Journal of experimental medicine · 2024Article
- Biphasic JNK-Erk signaling separates the induction and maintenance of cell senescence after DNA damage induced by topoisomerase II inhibition.Cell systems · 2023Article
- Molecular portraits of cell cycle checkpoint kinases in cancer evolution, progression, and treatment responsiveness.Science advances · 2023Article
- Article
- High glucose mediates apoptosis and osteogenesis of MSCs via downregulation of AKT-Sirt1-TWIST.Molecular biology reports · 2022Article
- Review
- Endothelial senescence mediates hypoxia-induced vascular remodeling by modulating PDGFB expression.Frontiers in medicine · 2022Article
- Article
- The Chk2-PKM2 axis promotes metabolic control of vasculogenic mimicry formation in p53-mutated triple-negative breast cancer.Oncogene · 2021Article
- Transcriptional coregualtor NUPR1 maintains tamoxifen resistance in breast cancer cells.Cell death & disease · 2021Article
- Natural podophyllotoxin analog 4DPG attenuates EMT and colorectal cancer progression via activation of checkpoint kinase 2.Cell death discovery · 2021Article
- Insight Into the Molecular Mechanism of Podophyllotoxin Derivatives as Anticancer Drugs.Frontiers in cell and developmental biology · 2021Review
- Article
- Phytochemicals inhibit migration of triple negative breast cancer cells by targeting kinase signaling.BMC cancer · 2020Article
- Convergence of therapy-induced senescence (TIS) and EMT in multistep carcinogenesis: current opinions and emerging perspectives.Cell death discovery · 2020Review
- Indolylkojyl methane analogue IKM5 potentially inhibits invasion of breast cancer cells via attenuation of GRP78.Breast cancer research and treatment · 2019Article
- Vimentin activation in early apoptotic cancer cells errands survival pathways during DNA damage inducer CPT treatment in colon carcinoma model.Cell death & disease · 2019Article
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Twist1, a basic helix-loop-helix transcription factor is implicated as a key mediator of epithelial-mesenchymal transition (EMT) and metastatic dissemination in p53-deficient cancer cells. On the other hand, checkpoint kinase 2 (Chk2), a major cell cycle regulatory protein provides a barrier to tumorigenesis due to DNA damage response by preserving genomic stability of the cells. Here we demonstrate that Chk2 induction proficiently abrogates invasion, cell scattering and invadopodia formation ability of p53-mutated invasive cells by suppressing Twist1, indicating Chk2 confers vital role in metastasis prevention. In addition, ectopic Chk2, as well as its (Chk2) induction by natural podophyllotoxin analog, 4'-demethyl-deoxypodophyllotoxin glucoside (4DPG), strongly restrain Twist1 activity along with other mesenchymal markers, for example, ZEB-1, vimentin and Snail1, whereas the epithelial markers such as E-cadherin and TIMP-1 expression augmented robustly. However, downregulation of endogenous Chk2 by siRNA as well as Chk2 selective inhibitor PV1019 implies that 4DPG-mediated inhibition of Twist1 is Chk2-dependent. Further, mechanistic studies unveil that Chk2 negatively regulates Twist1 promoter activity and it (Chk2) interacts steadily with Snail1 protein to curb EMT. Strikingly, Chk2 overexpression triggers premature senescence in these cells with distinctive increase in senescence-associated β-galactosidase (SA-β-gal) activity, G2/M cell cycle arrest and induction of senescence-specific marker p21
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.